The invention relates to a novel system for the diagnosis and treatment of pain such as pelvic pain.
Chronic pain is a significant and highly prevalent health condition that exceeds the cost burden of heart disease, cancer and diabetes in the United States. Women comprise a majority of all chronic pain populations, particularly persistent pelvic pain. As many as one in three women have some pelvic floor muscle disorder. Female chronic pelvic pain (CPP) is a rapidly growing health concern, consuming as much as $2.8 billion per year in health care services. CPP may reflect a number of underlying pain conditions including endometriosis, interstitial cystitis (IC), vulvodynia and pregnancy-related pelvic pain. CPP affects reproductive age women's physical ability, quality of life, psychological health and sexual function. Certain pelvic conditions, even if they do not cause pain, are responsible for undesirable effects such as incontinence. Men also suffer from CPP, from such underlying pain conditions as chronic prostatitis.
The current mechanistic understanding of CPP in women is not well understood in the prior art. Different types of CPP diagnoses often demonstrate overlapping clinical presentations, and the diagnosis often varies depending on which specialist is evaluating the patient. Given the lack of empirical evidence, treatment of CPP can be haphazard and indiscriminate, with few validated interventions emerging from significant research efforts.
Recent attempts have been made to revise diagnostic and treatment algorithms. For example, the UPOINT (Urinary, Psychosocial, Organ specific, Infection, Neurologic system, Tenderness of Skeletal Muscles) system for clinical phenotyping in women with CPP focuses on localized (organ) versus systemic differentiation. There have also been efforts to evaluate CPP by studying the overlapping comorbidities. However, even with these revised attempts to classify, scientific findings have failed to identify the causative mechanisms to guide treatment.
Treatment of CPP can be haphazard and indiscriminate, with few validated interventions emerging from significant research efforts. Recent attempts have been made to revise diagnostic and treatment algorithms. For example, the UPOINT (Urinary, Psychosocial, Organ specific, Infection, Neurologic systemic, Tenderness of Skeletal Muscles) system for clinical phenotyping in women with CPP focuses on localized (organ) versus systemic differentiation. There have also been efforts to evaluate CPP by studying the overlapping comorbidities. However, even with these revised attempts to classify, scientific findings have failed to identify the causative mechanisms to guide treatment.
Understanding the etiology responsible for CPP requires a dissection of peripheral and central pain mechanisms. Normal female pelvic physiology consists of somatic and visceral components that act alone and in tandem. Peripheral factors include sensory somatic (Aβ/Aδ mechanical nociceptors, unmyelinated C fibers), muscular, visceral and viscero-somatic crosstalk. IC patients have demonstrated bladder hyperalgesia and have altered response to thermal stimuli. Muscle tenderness has been reported in pregnancy-related pelvic pain. Animal models of pelvic pain have reinforced the role of increased sensory hyperinnervation, visceral afferent sensitization, and muscular tension, including parturition pain. Such peripheral changes are known to culminate in spinal cord (central) sensitization as pain transitions to chronicity. Alterations in brain function and structure in male and female pelvic pain have been shown. A comprehensive mechanistic understanding of female pelvic pain requires concurrent peripheral and central measures.
While a comprehensive mechanistic understanding of CPP does not exist, certain CPP subtypes are predominated by prototypical somatic features. Pregnancy-related CPP, for example, appears to be a purely somatic musculoskeletal subtype. It is localized, intermittent, and typically provoked by movement. The pathogenesis of this subtype is not known, but has focused on musculoskeletal etiologies with no effort made to study the sensory/peripheral neural or central influences. Other CPP subtypes are predominated by visceral features. IC, for example, represents a visceral CPP subtype dominated by a diffuse, constant, and often unprovoked pain presentation. Few studies have identified sensory or and muscular abnormalities in IC, and functional brain correlates to bladder distension have only been examined in healthy controls. Somatic and visceral components may act alone or in tandem.
Previous work in mechanical pressure sensitivity to Aβ/Aδ mechanoreceptors indicates that mean pressure pain detection thresholds at multiple vaginal sites are significantly lower in women with CPP (not pregnancy related) compared with healthy controls. The pelvic joints (sacroiliac joint and pubic symphysis) are thought to be the most common regional sources of postpartum CPP. Several clinical physical examination tests have been found to be sensitive and specific for pregnancy-related CPP especially when used in combination. Unfortunately, these examination maneuvers do not differentiate the exact peripheral nociceptors nor do they include vaginal pelvic floor muscle (PFM) assessment. Data indicates an association with sacroiliac pelvic pain and PFM tenderness. In a biomechanical model, the PFM appears to reduce the shear of the sacroiliac joint in a standing posture. In theory, this protective effect may be influenced by PFM injury during vaginal delivery. Preliminary data shows that most postpartum women with pelvic pain have PFM tenderness on vaginal examination compared to women without pain (FET). Indirect assessment of PFM kinematics has been conducted by abdominal ultrasound for somatic-musculoskeletal pelvic pain.
Pressure therapy is known in the art as a means of reducing pain in patients with pelvic pain. A pressure algometer may be used to measure a patient's sensitivity to pressure or to pain. Information obtained from such measurements is used in the art to identify an appropriate course of therapy for patients. For instance, applying pressure greater than a pre-determined threshold may result in pain improvement in patients. It is also known in the art that pelvic muscles, like other muscles in the body, generate varying amounts of electrical potential. Electromyography techniques with electrodes are used to evaluate and record the electrical activity produced by muscles (e.g. EMG signals).
Quantitative sensory testing (QST) is a standard approach to experimentally testing peripheral sensory abnormalities across diverse chronic pain populations. QST protocols have become standard measures in chronic pain states and alone they have failed to provide sufficient information about distinct pain mechanisms. However, CPP subtypes have received minimal to no attention (postpartum) in this respect, and existing studies have typically focused on few sensory modalities, rather than conducting comprehensive assessments of CPP sensory alterations. Peripheral nociceptors that relay pelvic pain signals include neuromuscular (i.e., Aβ and Aδ mechanoreceptors, unmyelinated C fibers) and visceral afferents, which can be segregated into pinprick, mechanical, thermal, and distension sensory modalities.
Considering the scope and importance of medical study on pelvic conditions and pelvic pain, relatively little research has focused on the development of objective measurements of optimal pressure to be applied to a pelvic area. Similarly, little research has been performed to determine baseline EMG signals of pelvic muscles, either in healthy patients or in patients with pelvic conditions.